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Bact/fungal path

Lecture11-12

QuestionAnswer
outcomes of encounter between microorganism and host infection and damageestablishment of a permanent relationshipinapparent/subclinical infectionprevention of infection or complete clearance
what influences the outcome microorganism's ability to breah host barriers and evade destructiontactics for replication, spread, establishment of infection, and causation of diseaseinnate and adaptive immunologic abilityability to transmit itself to a new susceptible host
stages in a pathogenic process exposure and entryattachmentinvasioneffects on the hostevasion of immune responsesdissemination
attachment adhesion=physical attachment to a cell or surfacebacteria can adhere to internal, external, or artificial surfacesnecessary first step in order to permanently colonize
factors that influence colonization ability to adherefavorable environmentpresence/absence of normal microflora/commensals
receptors for attachment can be specialized protein, component of a cellular membrane, surface component, or a general surface receptor
adhesins 1. Pili and finbriae: expressin may be coordinated with other virulence factors2. Afimbrial adhesions: ligands can be any cell structure
invasion not all bacteria have to enter host cells to replicatephagocytitic cells: enter by phagocytosisnon phagocytitic cells: many ways
invasins bacterial surface proteins that interact with specific receptors to induce endocytosis
host cell cytoskeleton rearrangement triggered by injection of bacterial proteins into host cell leading to membrane ruffling
Why are some infections inapparent/subacute? infected tissue is undamagedinfection is controlled before organism reaches its target tissuetarget tissue is expendable or rapidly repairedextent of damage is below a functional threshold
chronic/persistent infection microorganism continually detectable at low levelsmay have mild or no clinical symptoms (Typhoid fever)
latent infection virus not continually detectableintermittent reactivation leads to microorganism detectable/shed again (TB)
immunopathology damage to host cells as a result of the microbally induced immune response
direct damage cytolytic effecttoxinsphysical growthtoxic structuresdegradative enzymes
degradative enzymes produced by tissue damaging pathogensimportant in establishing spread, release of growth substrates1. hyaluronidase (breaks down hyaluronic acid of connective tissue)2. streptokinase (breaks down fibrin clots)3. collaginase (breaks down collagen)
toxic structures gram- LPSmultiple, concentration dependent effects
physical growth growth of hyphae push through cell walls and damage tissues
toxins exotoxinssecreted into extracellular environmentvery potent at low concentrationsgram + and -
Exotoxins toxic in small amountsspecific effectspolypeptidestoxoid formationno fever stimulationsecreted from live cellsgram+ and -
endotoxins toxic is high dosessystemic effects, fever, inflammationLPS in cell wallno toxoid formationcell lysis as releasegram- bacteria
benefits to the bacteria of exotoxin production diptheria: colonization of throat by killing polymorphs and epithelial cellscholera: resulting diarrhea aids in transmissionpneumolysin: interfers with host defenses
Class I exotoxin surface acting
Class II exotoxins membrane acting
Class III exotoxins intracellularA: catalytic (Active) domainenzymatically attacks a particular host cell function or structureB: Binding subunitlinked to A by disulfide bondspecific host cell glycoprotein or glycolipid
entry of exotoxin 1. binding to specific receptor on target cell2. entry via RMA or via pores3. internalization--> specific activity at defined target site
ADP ribosylation addition of ADP ribosyl group onto functional cell protein--> change in function/activation of the target proteinex. diptheria toxin: expression triggered by low levels of iron, target: EF-2
Pore formation channel forming toxins (class II exotoxin)has many targetscell death occurs due to osmotic lysis or apoptosisprotein pores destabilize cell membrane
phospholipid membrane destabilization class II exotoxinsindiscriminate lysisdestabilize cell membrane by removing polar head group from phospholipids
zinc metalloprotease proteolytic cleavage of toxin-->2 linked fragments1. Light chain-enzymatically active2. Heavy chain-binding and translocation
Tetanus toxin produced by clostridium tetanitargets inhibitory interneurons in CNSlight chain targets membrane component of synaptic vessicleinhibition of inhibitory neurotransmittersleads to spastic paralysis
Botulinum toxin produced by clostridium botulinumtargets presynaptic motor neurons (PNS)light chains target membrane component of synaptic vesiclesinhibition of ACh releaseflaccid paralysis
toxin based vaccines toxoid=inactivated exotoxinstill antigenic, but cannot cause damagediptheria/tetanus (examples)
pathogenicity islands clusters of genes encoding for virulence factors such as:toxinssuperantigensiron uptake system/siderophoresadhesinspresent in pathogens but missing in same non-pathogenic speciesassociated with mobile genetic elements
coordination of virulence gene response two component signal transduction systemcoordinate bacterial responses to environmental stimulisensor in cytoplasmic membrane, response regulator in cytoplasm
how bacteria obtain iron synthesis of surface receptors that can grab the host's iron chelatorssynthesis and secretion of siderophores (low molecular weight and high affinityfor iron)
evasion of complement capsules, complement binding proteins, proteases, host cell mimicry
evasion of phagocytic killing capsules, type III secretions, intracellular parasitism
evasion of antigen processing interfere with MHC function and antigen processing
evasion of antibodies Ig-binding/inactivating proteins, antigenic variation
evasion of apoptosis decoy proteins
capsule composition polysaccharide, polyribose ribitol phosphate, hyaluronic acid (host cell mimicry)
toxins to kill macrophages and leukocytes leukocidins-->kill neutrophils and macrophagesalters phospholipid metabolism by ADP ribosylation of a protein controlling phosphotidylinositol-->disruption of cellular activitiesproduced by highly invasive bacteria
phagocytic killing solution: replicate in phagocytic cellsprevent fusion of phagosome & lysosome (legionella)escape into cytosol (L. monocytogenes)resist lysosomal enzymes (histoplasma)inavtivate harmful O2 species (s.aureus)
Ig-binding/inactivating proteins bacterial IgA proteases inactivate sIgA by proteolysisdirect binding of bacteral cell wall protein to Fc domain of IgG
Antigenic/phase variation antigenic variation=multiple antigenic forms can be expressed at different timesphase variation=can switch protein expression on and off
biofilm formation bacterial and/or fingal attachment to a tissue/artificial surface and production of a covering layer of EPS
dissemination enables movement to another site within the body
direct movement surface fluids, flow of intestinal contents, facilitated by toxin production, growth through tissues
via nerves not generally used by bacteria or fungi
CSF cross blood CSF junction, requires movement into bloodstream first
Blood in blood or blood components
lymphatics from tissue fluids into lymphatic capillaries
transmission route by which microorganisms are transfered from a reservoir to a new host
transmissibility number and period of time organisms are shed for
routes of transmission vertical, direct, droplet, fecal oral, sexual, environmental, vector borne
Created by: kamarsh